Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes

Uncini, Antonino; Manzoli, Claudia; Notturno, Francesca; Capasso, Margherita

doi:10.1136/jnnp.2010.208538

Cited by 180 publications

(211 citation statements)

References 39 publications

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“…This is a highly speci fi c fi nding but is found in only about one-third of patients with GBS, dependent on the number of nerves and nerve segments studied [ 95,98,100 ] . Conduction block is often a sign of segmental demyelination, but transient conduction and block may be seen as the early manifestations of axonal loss such during the early stages of AMAN [ 105,106 ] . Sequential studies are necessarily before a fi nal diagnosis of axonal loss is made.…”

Section: Motor Conduction Blocksmentioning

confidence: 99%

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Guillain-Barré Syndrome and Related Disorders

Piccione

Salame

Katirji

2013

Neuromuscular Disorders in Clinical Practice

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Section: Motor Conduction Blocksmentioning

confidence: 99%

“…Also, low distal CMAPs may be due to distal demyelination with distal conduction block and often mimic axonal loss. Rapid recovery of low distal CMAPs and SNAPs on sequential studies is a necessary con fi rmatory sign of distal demyelination [ 106 ] .…”

Section: Motor Conduction Blocksmentioning

confidence: 99%

Guillain-Barré Syndrome and Related Disorders

Piccione

Salame

Katirji

2013

Neuromuscular Disorders in Clinical Practice

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“…Dette kan medføre en underdiagnostisering av akutt motorisk aksonal polynevropati til fordel for akutt inflammatorisk demyeliniserende polynevropati. Kontroll av EMG/nevrografifunn etter noen uker er anbefalt (17,18).…”

Section: Perifere Nervesykdommerunclassified

Elektromyografi og nevrografi ved alvorlig nevromuskulær sykdom

Løseth¹,

Torbergsen²

2013

Tidsskriftet

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Elektromyografi og nevrografi ved alvorlig nevromuskulaer sykdom 174 -8 Sissel LøsethKUNNSKAPSGRUNNLAG Artikkelen er basert på forfatternes kunnskaper og erfaringer, med spesiell vekt på metodenes anvendelse i utredningen av alvorlige sykdommer i tverrstripet muskulatur og i perifere nerver. Det ble gjennomført et litteratursøk i PubMed med begrensning 15 år bakover i tid. I tillegg har vi gjort et skjønnsmessig utvalg av artikler som vi kjente til.RESULTATER Ved utredning av myopati er EMG mest verdifull, og ved nevropati gir nevrografi mest informasjon, men metodene utfyller hverandre. Ved enkelte tilstander er undersøkelsene de mest sensitive for diagnosen (for eksempel myasteni). Høy kompetanse er nødvendig for diagnostisering av de omtalte tilstandene.FORTOLKNING EMG og nevrografi er viktige og ofte nødvendige undersøkelser i utredning av pasienter med alvorlig nevromuskulaer sykdom.

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“…This could lead to the misdiagnosis of AMAN as AIDP and may have some impact on the reported prevalence of the different forms of GBS in epidemiological studies . Also, timing of electrophysiological studies during the illness course might be of importance, with axonal features being more prominent later in the disease course, when secondary degeneration of axons of demyelinated nerve fibres is not uncommon (Uncini, Manzoli et al 2010). …”

Section: Overlap Syndromesmentioning

confidence: 99%

“…For example, conduction block, a neurophysiological finding typical of demyelination, can be present in axonal disease if blocking of the nodes of Ranvier occurs (Uncini, Manzoli et al 2010). This could lead to the misdiagnosis of AMAN as AIDP and may have some impact on the reported prevalence of the different forms of GBS in epidemiological studies .…”

Section: Overlap Syndromesmentioning

confidence: 99%

Immunogenetic studies of Guillain - Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Blum¹

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Guillain-Barre syndrome (GBS) is an acute inflammatory neuropathy that is frequently triggered by an infectious illness. It is thought to be autoimmune in origin, but differs from other autoimmune diseases in being of male predominance and not showing a HLA-association.Chronic inflammatory demyelinating polyradiculoneuropathy is a chronic inflammatory neuropathy, which shares some pathological features with GBS.We investigated the clinical features of GBS in an Australian cohort of subjects by performing a retrospective chart review. We obtained subjects from several public hospitals and private neurologists in Queensland and New South Wales.We found 335 patients, for 228 of whom electrophysiological data was available. Of these acute inflammatory demyelinating polyradiculoneuropathy (AIDP) with 168 cases was the most common form, whilst axonal and focal forms were rarer. We identified upper respiratory tract infections, occurring predominantly in winter months, as the most frequently named triggering factor for GBS.The illness severity in our cohort was similar to that in earlier Australian studies.Also, we identified a cohort of 78 subjects fulfilling diagnostic criteria for CIDP from similar sources.We investigated a possible underlying genetic susceptibility to develop GBS or CIDP by contacting members of this cohort and collecting their DNA. We embarked on both a candidate gene approach to investigate the killer immunoglobulin-like receptors (KIRs) and their HLA ligands, as well as performing a genome-wide association study (GWAS) of the subjects with GBS as a hypothesis-free method.For the KIR/HLA system, whilst no significant differences were detected in the frequency of KIR genes, HLA-C2 and HLA-B Bw4-T were more frequent in subjects with GBS than controls (p<0.001). The inhibitory pairs of KIR-2DL2/HLA-C2 and KIR-3DL1/HLA-B Bw4-T were more frequent in GBS than controls (p<0.005). Whilst there were some differences between CIDP subjects and controls, interestingly, there were no difference between subjects with GBS and CIDP.This could point to similarities of pathogenesis between these two inflammatory neuropathies.A GWAS was performed on a largely identical cohort of 190 subjects with GBS. Whilst this cohort is relatively small for a modern GWAS and no genome-wide significant results were expected, we were able to identify a number of regions of interest based on clusters of SNPs in linkage disequilibrium of increased significance. These included rs10519519 on Chromosome 2, which is associated with MYT1L, a transcription factor in neuronal development; rs7663689 on Chromosome 4, which is in the promotor region of IL15; rs11151180 on Chromosome 18 which is in a gene-free region; rs17095496 on Chromosome 14, which amongst other genes is associated with DACT1, which encodes a regulator of cell division involved in the NF-κB pathway; and rs2302524 on chromosome 19, associated among other genes with NFKBIB, which encodes an inhibitor of the NF-κB pathway. Relative negatives included the HLA region, a...

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Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes

Cited by 180 publications

References 39 publications

Guillain-Barré Syndrome and Related Disorders

Guillain-Barré Syndrome and Related Disorders

Elektromyografi og nevrografi ved alvorlig nevromuskulær sykdom

Immunogenetic studies of Guillain - Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

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